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A chilli for your pain

A chilli for your pain

Capsaicin, a chemical found in chillies, is known to have pain-relieving effects. It burns at first but eventually numbs the tissue and has been in use for long as an analgesic that is applied locally to a part of the body, like pain-relieving creams and gels, nasal sprays and dermal patches. However, researchers did not have an understanding of the action of this compound.

A new study in Science Signalling by Istvan Borbiro and colleagues from Rutgers University’s New Jersey Medical School in Newark gives an insight into how capsaicin mediates pain relief.

The researchers studied sensory neurons involved in pain perception from the dorsal root ganglion (cell bodies of sensory neurons that bring information from the periphery to the spinal cord) and discovered that capsaicin’s activation of one type of ion channel in the neurons inhibited the activity of another type of ion channel. Specifically, the researchers show that the initial sensation of pain being dulled occurs when capsaicin activates signalling by heat-sensitive transient receptor potential vanilloid 1 (TRPV1) ion channels. This signalling blocks the pressure-sensitive mechanically activated (MA) channels known as Piezo1 and Piezo2. According to the researchers, the activation of TRPV1 channels inhibited the neurons’ MA channels by depleting lipids known as phosphoinositides in the cells’ plasma membranes. Prolonged activation by the compound results in desensitising these neurons. TRPV1 is a heat sensor. So how it affected mechanical pain was not known. Now we know that it is the blocking of the mechanically activated piezo channels by TRPV1 channels which results in the analgesic effect.

The unique finding of this study is how one kind of channel regulates the activity of another. This is believed to be the first example of ion channel cross-talk mediated by phospholipids.

It should also be pointed out here that a study in 2010 found that capsaicin also had a co-carcinogenic role in skin cancer, which is mediated through the epidermal growth factor receptor (EGFR) and not the pain receptor TRPV1 whose activation has a positive analgesic effect.

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